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PR3136 > ANTI-PARKINSON DISEASE > Flashcards

ANTI-PARKINSON DISEASE Flashcards

1
Q

Young onset parkinson’s disease

A

21-40y/o

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2
Q

Juvenile onset parkinson’s disease

A

=< 20y/o

- higher frequency of genetically inherited PD

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3
Q

Pathophysiology of PD

A
  • Impaired clearing of abnormal/damaged proteins by ubiquitin-proteasomal system
  • Accumulations of toxic proteins, aka aggresomes or lewy bodies, leading to apoptosis of dopaminergic neurons in substantia nigra
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4
Q

What does lewy bodies contains?

A

alpha-synuclein & ubiquitin

lewy body eosinophilic cytoplasmic inclusions

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5
Q

Why is the degeneration of dopaminergic neurons in substantia nigra important?

A
  • Substantia nigra has dopaminergic projections into the basal ganglia
  • Basal ganglia is important to facilitate and modulate movements initiate by motor cortex
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6
Q

Diagnosis of PD

A 
No reliable diagnostic marker for PD
Hence, 
1. Presence of clinical features
2. Elimination of alternative diagnosis
eg atypical parkinsonian disorders
3. Neuroimaging of dopaminergic neurons in substantia nigral
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7
Q

Parkinson’s disease = Parkinsonian syndrome?

A

No

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8
Q

3 cardinal features of PD

A
  1. Rest tremors
  2. Rigidity
  3. Bradykinesia
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9
Q

Non-motor manifestation of PD (4)

A
  1. Autonomic (postural hypotension & instability)
  2. Neuropsychiatric
  3. Olfactory
  4. Sensory
  • relatively resistant and may be worsened by dopaminergic agents (eg Levodopa, MAO-B, Dopaminergic agonist)
  • more prominent in later stages of disease
  • significant disability
  • common in PD
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10
Q

Progression of disease

A
  • progressive disease
  • rate of disability progression is most marked in early years of the disease, before plateauing
  • significant disability 10-15 years after onset
  • patients become increasingly dependent in their daily activities
  • motor fluctuations, dyskinesia & non-motor symptoms are more common at later stages
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11
Q

How to decide what medications to use? (6)

A

Individualised

  1. age
  2. stage of disease
  3. level of activity
  4. psychological conditions
  5. associated medical conditions
  6. patient factors (eg occupation)

Start low, go slow

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12
Q

Early symptomatic disease without complications

A
  • may not even need to start medications if coping well
  • emphasize non-pharmacological (4) :
    1. stretching & maintaining balance and posture
    2. healthy and balanced diet
    3. knowledge on disease
    4. social support

HOWEVER, rate of disability progression most marked in early years of the disease

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13
Q

Classes of anti-PD drugs (6)

A
  1. Levodopa +/- peripheral decarboxylase inhibitor (benserazide/carbidopa)
  2. Anticholinergics (trihexyphenidyl - Artane)
  3. MAO-B inhibitors (selegiline - Jumex)
  4. COMT (Entacapone & Tolcapone)
  5. Dopamine agonist (Bromocriptine, Pergolide, Pramipexole, Piribedil, Ropinirole)
  6. Amantadine
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14
Q

Treatment for mild PD

A

MAO-B inhibitors (selegine - Jumex)

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15
Q

Treatment for young patients with PD

A

Dopamine agonists > Levodopa

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16
Q

Levodopa MOA

A
  • dopamine precursor
  • 2-in-1 preparation with peripheral decarboxylase to increase levodopa uptake by brain
    benserazide or carbidopa
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17
Q

ADR of Levodopa

A

Short term :

  • n/v
  • postural hypotension

Long term :
- motor fluctuations
- irreversible tardive dyskinesia (10%/year)
Hence, even though it is gold standard, the dose of levodopa must be kept to minimum.

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18
Q

Why must the dose of Levodopa be kept to minimum? How?

A

This is because Levodopa can cause irreversible tardive dyskinesia (10%/year)
Dose of Levodopa can be kept minimum by adopting adjunct therapy with :
1. Anti-cholinergics
2. COMT
3. Dopamine agonists

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19
Q

Anti-cholinergics MOA

A
  • symptomatic treatment to control tremors

- peripherally acting agents can use for sialorrhoea (excessive salivation)

20
Q

ADR of anti-cholinergics

A
  • dry mouth
  • sedation, blurred vision
  • constipation
  • urinary retention
  • insomnia, confusion, hallucinations, delirium

esp in elderly

21
Q

Example of anti-cholinergics

A

Trihexyphenidyl (Artane)

- 2-15mg/day

22
Q

Anticholinergics for PD

A
  1. Symptomatic monotherapy

2. Adjunctive therapy to Levodopa

23
Q

MAO-B inhibitors MOA

A
  • inhibit MAO-B from breaking down dopamine
  • increase synaptic dopamine
  • may delay the dopaminergic nigral brain cell degeneration
24
Q

ADR of MAO-B inhibitors (7)

HAPICNV

A
  1. heartburns
  2. anxiety
  3. palpitation
  4. insomnia
  5. confusion
  6. nightmares
  7. visual hallucinations
  • loss of appetite
  • n/v
  • constipation
  • dizziness
  • headache
25
Q

Example of MAO-B inhibitor

A

Selegiline (Jumex)

26
Q

MAO-B inhibitors for PD

A

Symptomatic monotherapy in early PD for mild parkinsonian activity

27
Q

COMT MOA

A
  • Catechol-O-methyltransferase inhibitors
  • blocks enzyme that converts Levodopa to inactive form, hence extend the duration of action of Levodopa
  • increase levodopa available to enter brain
  • only effective if used with Levodopa
28
Q

ADR of COMT (6)

A
  1. Increase abnormal movements (dyskinesia)
  2. Liver dysfunction (Tolcapone)
  3. Urine discoloration
  4. N/V, diarrhoea
  5. Visual hallucinations
  6. Daytime drowsiness & sleep disturbances
29
Q

Examples of COMT (2)

A
  1. Entacapone

2. Tolcapone

30
Q

Dopamine agonists MOA

A
  • bind to dopamine receptors in brain to reduce symptoms of PD
  • anti-PD effect not superior to levodopa
  • prevent / delay onset of motor complications
31
Q

ADR of Dopamine agonists (6)

A
  1. Similar to Levodopa
  2. “ergot” derivative - fibrosis
  3. arrythmias
  4. somnolence (pramipexole & ropinirole)
  5. pedal edema
  6. restrictive valvular heart disease (pergolide)
32
Q

Examples of Dopamine agonists (5)

A
  1. Bromocriptine
  2. Pergolide (RVHD)
  3. Pramipexole (somnolence)
  4. Piribedil
  5. Ropinirole (somnolence)
33
Q

Dopamine agonists for PD

A
  1. Symptomatic monotherapy
  2. Adjunctive therapy to Levodopa

For younger patients, dopamine agonists > levodopa as first line

34
Q

Amantadine MOA

A
  1. Dopamine receptor agonists
  2. Release stored dopamine into synapse
  3. Inhibit pre-synaptic reuptake of catecholamines
  4. NMDA receptor antagonists
35
Q

ADR of Amantadine (6)

A
  1. Psychological (anxiety, suicidal ideations, insomnia, schizophrenia)
  2. Seizures
  3. SJS
  4. Livedo reticularis (venule swelling due to thromboses)
  5. Cognitive impairment
  6. Hallucinations & nightmares
36
Q

Benefit of Amantadine

A
  • anti-dyskinetic (used for patients w motor fluctuations)
37
Q

Initial clinical indications of Amantadine

A

anti-viral

38
Q

Advantage of MAO-B inhibitor (Selegiline)

A
  • may delay the degeneration of nigral brain cells
39
Q

Advantage of COM-T inhibitors (Entacapone & Tolcapone)

A
  • Increase the duration of action of each dose of levodopa

- Beneficial for “wearing off” responses

40
Q

Advantage of Dopamine Agonists

A

Delay or prevent the onset of motor complications

41
Q

Livedo reticularis

A
  • venule swelling due to thromboses

- mottled reticulated discolouration of limbs

42
Q

Drugs and their advantages (4)

A
  1. MAO-B inhibitors
    - delay the degeneration of nigral brain cells
  2. COM-T inhibitors
    - extend the duration of action of levodopa for each doses by inhibiting the conversion to inactive form
  3. Dopamine agonists
    - delay the onset of motor complications (anti-dyskinetic)
  4. Amantadine
    - anti-dyskinetic (used for patients w motor fluctuations)
43
Q

Mild antiparkinson activity

A
  1. MAO-B inhibitors

2. Amantadine

44
Q

Any significance prevalence rates of PD between races

A

No

45
Q

Average onset of PD

A

early-mid 60s

46
Q

Anti-dyskinetic vs Delay/Prevent onset of motor fluctuations

A

Anti-dyskinetic

  • reduce motor fluctuations
  • used if patients have motor fluctuations
  • amantadine

Delay/Prevent onset of motor fluctuations

  • used before patients have motor fluctuations
  • dopamine agonists

PR3136 (19 decks)

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